BONUS: Lipid Masterclass: An Introduction to Lipids and Cholesterol with Dr. Thomas Dayspring

Welcome to Everyday Wellness Podcast. I'm your host, nurse practitioner, Cynthia Thurlow. This podcast is designed to educate, empower and inspire you to achieve your health and wellness goals. My goal and intent is to provide you with the best content and conversations from leaders in the health and wellness industry each week and impact over a million lives. This is bonus Monday, your most downloaded favorite podcasts. I love that this community runs the gamut from medical professionals, research scientists, science writers, personal trainers, and more. These are your favorite most loved podcasts in the last five years. I could not be more proud of the diversification of guests that appeal to all of you. Thanks for tuning in. This episode of Everyday Wellness is the first in a series of lipid master classes with the incredible Dr. Thomas Dayspring, who is a fellow of both the American College of Physicians and the National Lipid Association and is certified in internal medicine and clinical lipidology. He has served as educational director for nonprofits and has previously served as a chief academic advisor for two major cardiovascular labs. He is an absolute delight and because of the in-depth conversation that Dr. Dayspring and I have had over a series of multiple conversations, nearly six hours in length, it made the most sense to break these lipid master classes into chunks to make it easier to understand. If you are listening right now, you may want to go back and dog tag this podcast episode and listen to it several times. In this first episode, we discuss what are lipids, the classification of lipids and fatty acids, the physiology of cholesterol as well as transportation, the role of apoptosis, apoproteins, and apolipoproteins, differences between HGL, LDL, IDL and VLDL, how to calculate LDLs and triglycerides, looking at clues for poor metabolic health, his preferences in terms of lab values, and clues to determine or to provide information about early cardiovascular disease risk. This episode is a bit heavy and physical chemistry. However, I do make sure as I'm weaving through the conversation, I'm picking up the clinical pearls to make it easier to understand. Again, this is a first master class in a series. Stay tuned for the rest. I'm really excited you're joining us. Welcome, Dr. Dayspring. I'm so grateful and so appreciative of the work that you do and really excited to introduce you to my everyday wellness community. Well, I'm very happy to be here, Cynthia. You know, it's so funny because we contacted each other and without really knowing too much about each other and alone behold, we're actually probably within 10 miles of each other where we live in central Virginia. So even though this is a virtual podcast, I could have usually driven down to you to studio and looked at you in person. So this should be a lot of fun. Absolutely. Absolutely. And to give listeners some context to the topics we're going to be exploring today, let's talk a little bit about basics, lipid biology. What exactly are lipids? Why are they important? Because I think over the past 50 or 60 years, there's been a lot of emphasis on fearing the role of cholesterol. A cholesterol is very important in the body. And I know you are an expert in talking about lipids and good manage and lipidology. So let's start with the basics to kind of give our listeners and our community some context to some of the discussions that we're going to have today and moving forward. Sure. Well, the first thing is absolutely to define what the heck is a lipid. You know, biochemistry is full of a lot of molecules, all of which perform various functions. You're so in many of them in the animal kingdom. And certainly cholesterol is one of the lipids that is absolutely crucial for human life and certain amounts beyond that it can cause harm to lower can cause harm. So lipids are basically oils. And what that means is they are molecular compounds that are not soluble in water. Everybody knows, pour some olive oil in the glass of water and it's not missable. It doesn't circulate. It floats on top. So this does create certain physical chemistry attributes in the human body because lipids have to traffic from one cell to another. And the only way lipid's traffic is in our bloodstream, our plasma, which happens to be what scientists would call an aqueous solution, meaning it's water. So how in the world do these things that hate water? That's called hydrophobic molecules, lipids do they circulate in water? So evolution had to solve that problem and we'll get into that soon. The lipid category, they're actually organic molecules, which means they are carbon hydrogen and oxygen atoms. Perhaps with another atom here, they're attached to it. But they're stuck together in various joints, ways of constructing macro molecules and they form this whole class of lipid molecules. The lipids that are most talked about by laymen when they see their doctors or by physicians or clinicians like yourself are cholesterol, of course. But cholesterol is just one of many other stirrals. So stirrals are a big classification of lipids. Cholesterol is obviously talked about the most, but there are 40 or 50 other ones. All of those other ones are grouped in a name called non-cholesterol stirrals. I prefer the term xenostirals. The xenomines other in Greek. So other stirrals that are not cholesterol. And believe it or not, they play big roles also in the human body. And they also, you know, it's not only the animal kingdom that has cholesterol and other stirrals in it, but the plant kingdom does also. And most of the stirrals that are in plants are not cholesterol. That's pretty much in the animal kingdom. We call that a zooo stirrall. And of course, the stirrals that are in plants are called phytosterols, no surprise. So we have cholesterol, a bunch of other stirrals, and you got a big group in called phytosterols. The other lipids, of course, of interest to everyone, including clinicians, are fatty acids. And fatty acids are also crucial for human life. The good news is other than a two or three of them, the human body can denobosynthesize all of the fatty acids it may meet or so. So there's only a couple of essential fatty acids that you have to eat that the body would have very tough trouble synthesize. And there, as you know, the omega-3 class of fatty acids or so. I'm sure sooner or later we'll touch on them. The other fatty acids are important because we eat them, they get absorbed, and they're then used again. Many of the fatty acids, the one that mostly affects cardiology and afterscrotic risk, are fatty acids to just create efficiency, are traffic bound together. So if I take a backbone molecule that can attach to fatty acids, and that's called glycerol. Glycerol is a three-carbon sugar. Won't you? If you saw the you'd see three carbons, and of course you can stick things onto those carbons. So if I stuck two fatty acids onto a glycerol molecule, and I stuck another molecule that has a phosphorus moiety in it, I just created a phospholipid. Phospholipids are two fatty acids on glycerol with a head group that has phosphorus in it, and there are many of those head groups. Super crucial to the human body, because phospholipids make up virtually all of our cell membranes, and they contribute to the functionality of our cells. That means are we going to have healthy cells, or not so healthy cells, and the phospholipid construction has everything to do with that, and most important to the phospholipids are which fatty acids are stuck at them, and which phosphorus head group is on them too. Phospholipids are the lipid molecules that are least understood in the clinical community, unless you go into advanced lipidology, they're not talked a lot about, and the reason why is we don't typically measure phospholipids in the bloodstream when we do lipid analyses on people. But you'll hear me talk about them because they are kind of super crucial to where I'm going. And of course the last lipid molecule, and everybody knows about this, and the dark ages it was dismissed as, oh that's not important in nowadays, in our little insulin resistant world, it's become a crucial lipid. So if I take that glycerol molecule with three carbons, and I stick three fatty acids on it, the biochemical for fatty acids is acyl. So if I took three acyl groups, three fatty acids and stuck it on a glycerol molecule, I would have tri acyl glycerol, better known to the world as triglycerides. It's funny when I started back in the dark ages of the 1960s, they were just simply called glycerides, and the term triglycerides evolved as well, a triglyceride is really a phospholipid and a triglyceride, it's a way for three fatty acids to get in. Now most of the fats that we eat animal fats are in the form of a triglyceride. So we chew, maybe it's a piece of meat, maybe it's whatever, and income those triglyceride molecules. They're pretty monstrous molecules with glycerol and three, many oftentimes long chain fatty acids stuck on to them. So they are unobsorbable, and evolution had to figure, oh my god, we got to get these fatty acids into the body, some of them are important, especially those Omega's, and so we were given a pancreas. And pancreas, when we eat, our body signals the pancreas, hey shoot out some enzymes, the gut is going to need to dissolve certain macro molecules that we eat so they can be absorbed. So the pancreas shoots out a whole class of enzyme called light paces. Light paces dissolve fatty acids from glycerol. We have phospholipaces that digest eaten phospholipids, and we have triglyceride light paces, lipoprotein light paces, whatever you want to call it, intestinal light paces. And what that does is we swallow those big three fatty acids on a glycerol, it starts cleaving the fatty acids off of the glycerol. So now simple fatty acids are easily absorbed by intestine, and the intestine has a membrane transported that recognizes the fatty acids and pulls them into your intestinal cells. Likewise, most of the cholesterol we eat is also in an astrophide form, which means yes, it's a cholesterol molecule, but it's bound to usually a long chain fatty acid. That's called cholesterol if you listen to my pronunciation's cholesterol, ill-estor, YL, not OL, esters, YL is the biochemistry of radiation. So if we swallow this big monstrous cholesterol, cholesterol molecule, the pancreas shoots out a cholesterol, Esterolase, another light paces, and it cleaves the fatty acid off of the cholesterol, and what you have in your intestine, aluminum now is called free cholesterol, and that is easily absorbed. There's a specific transporter looking to bind to cholesterol, and it'll pull it in. Just then aside, the receptor that pulls in cholesterol is a very different receptor than what pulls in fatty acids. Hergo absorption of cholesterol has nothing to do with absorption of fatty acids, but all the way as lipids get into our enterocytes, but we're a complicated little machine, including our intestine. So that was a long answer on what the heck lipids are, given you the major classes that I'm sure we're going to elucidate more about herself, but they're just little oily molecules that I showed you how to get in, and now once they get into the intestine or if cells are making them, how in the world did they jump from one cell to another in the plasma? So I'll stop there and then I'll show you how many of you answer that question, or you can point me in another direction. If you're in perimenopause or menopause and are feeling more fatigued, dizzy, lightheaded, struggling with headaches or noticing your workouts feel harder than they used to, electrolytes may be part of the missing piece. As estrogen declines, we lose some of the fluid regulating and vascular protective effects that hormones once provided. 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I think that there's this presumption that we chew food, we swallow it, and that it instantaneously magically gets to where it needs to be. So this explains why individuals that are lacking lipase or perhaps their bodies not making as much can contribute to fat malabsorption and some of the clinically some of the issues that we see. So, you know, we talked about a little bit about lipid biology. Let's talk about how we these lipoproteins actually move you these little transportation vehicles that we have in the body. And I love the analogies to thinking about them like machinery or cars because it helps people understand because these can be some complicated concepts helping people understand that lipids and proteins how they get around the body to where they need to be. You mentioned they're absorbed into the gut loom in with specific enzymes and carrier molecules, but let's talk a little bit more about how we go from talking about phospholipids, phospholipid bilayers, triglycerides, esters, etc until we're actually talking about the transportation system in the body. Yep. So basically, I've led in this journey, we're going that you got these lipid molecules floating in your intestine. If the pancreas has done the proper enzymes, you have a lot of lipid molecules that the body has to make a decision. Should I absorb them or should I not? And obviously, it's always going to absorb exomel. Hopefully not overabsorbed, but unfortunately that can happen. Or hopefully not underabsorbed because as you sort of use the word malabsorption, you don't want to own the absorb lipids or that might cause some problems. So basically, I told you how some lipid molecules get into the intestinal cells. They're called the enterocytes. They line the intestine. But so what? They're in cells. What if another cell in the body needs some of those fatty acids or the cholesterol you just absorb? How in the world do they get there? So one little aside before I answer that magical question is of course, every cell in the body can certainly make all the cholesterol it needs. There is no cell that actually constantly requires a supply of cholesterol to get it to it. Now, I mentioned fossil lipids are so crucial because they line every cell membrane, but not by themselves. In betwixt fossil lipid molecules is another essential lipid that makes the cell membrane totally functional. And guess what? It's cholesterol. So your cell membranes not only need fossil lipids, they need cholesterol, a certain amount in betwixta fossil lipids. And if we all all have the right type of fossil lipids aligned on the surface of ourselves and there are interspace cholesterol molecules, we will have functional cell membranes. And what functional means is the membrane allows certain receptors to be placed strategically in the membrane. And those receptors can either pull in substances that the cell needs or if the cell has some garbage, these transporters on the membrane can evict stuff that the cell wants to get rid of. But of course, if it evicts it, it's got to put it in something. It doesn't just dump it into our blood stream. So that's the fossil lipid cholesterol cell membrane story. One thing just for accuracy, you did mention a word by layer. What that means is think of the cell as a balloon. So on the surface is all these fossil lipid molecules, but they're aligned. There's a outer layer that interfaces with the water in the plasma. And then they join another layer of fossil lipids. And it's the fatty acid tails that interlock with each other. So the outside of the fossil lipid membrane is partially water soluble. That's the phosphorous moiety. And then the inside is also got the phosphorous moiety because it interacts with the cytosol of the cell, which is pretty much another aqueous miliou also. So by layer of fossil lipids with intermixed cholesterol molecules. And hopefully you got the essential phosphorous lipids and the right amount of cholesterol. Now I did mention cholesterol is necessary for human life. Absolutely. You've got to have X amount each cell has to have X amount of cholesterol because it's how it gets in the cell membrane. The cell makes it and it just translocates truly cytosol and jumps into the membrane. All right. But what happens if for some reason there's the wrong type of substrates in that cell and it overproduces cholesterol? It's got more cholesterol molecules than it needs. Cholesterol in physiologic amounts is thank you Jesus. We need that for normal function. But excess cholesterol is incredibly toxic. It crystallizes and it kills the cells. The medical term for that is apoptosis. You really don't want your cell's dying prematurely. So the last thing you want in any cell is excess cellular cholesterol. Good news evolution knew that would be a problem. So it said if any cell has excess cholesterol, we have a cholesterol E-flux protein which the cell can make. It will relocate at the cell membrane and it will take excess free cholesterol and E-flux it out to oh you got to have a cholesterol acceptor. So here's where how these lipid molecules traffic through plasma. The acceptor molecule for lipids is a protein. You sort of indicated that proteins are the carrier for lipids in plasma. Proteins are soluble in an increase in water medium. So if our cells got too much lipids, it can evict them. They're attached to proteins and some of the proteins they attach to are big enough to accept several lipid molecules and once lipids are surrounded by proteins, you have a water soluble lipid transportation vehicle. Now I gave you the anatomy of the cell. Let's take these big lipoproteins are pretty much circular protein in wrapped molecules. So on the surface you got the big protein that makes them soluble in water and then you have a conglomeration of lipids. What is the outer layer of this lipoprotein macromolecule I'm describing? Guess what? It's phospholipids and free cholesterol. The same thing that lines our cells except on a lipoprotein it's a monolayer. It's not a bilayer. So you have a simple layer of phospholipids and free cholesterol. They have some water solubility and that's why they're on the surface of a lipoprotein. Inside the lipoprotein particles what we call the core and that's where all the water heating lipids, the hydrophobic lipids will be carried and they are cholesterol ester cholesterol at a fatty acid attach and triglycerides. So now you got this balloon that is water solubility because of its covering of phospholipids and proteins. Inside few of us remember back in probably grammar school or high school we were taught how to calculate the volume of various shapes. The volume of a sphere a circular molecule is a third power of the radius. So it doesn't take even incredibly minimal changes in the radius. Translates in the ability to carry several thousand more lipid molecules. So a third power of the radius. I bet most people don't know it takes 16 marbles to fill a ping pong ball. You would take it and it would take two or three marbles but because it's the third golf ball it's a bigger. Not that much bigger but the radius if you do a cube of it can take a lot more volume and that's why when we talk more about these lipoproteins some of them are really big big balloons and some are real tiny and will explain why evolution made some tiny and some big as we talk more importantly about lipid transportation in the aqueous plasma. So the protein that accepts cholesterol out of all the cells in our body exterior to the brain. The brain has a it's own lipid transportation system which has almost nothing to do with what's going on in the plasma and I hope either in this one or a future podcast we can spend some time up in our nogins because they're pretty important and we're just basically in our infancy understanding lipids in the brain. So that is well worth another talk down the road but you got to know the basics before you cross that blood brain barrier and start seeing what's going on up there. So if I'm a cell and I've made too much cholesterol and I said oh my god I'm going to die unless I can evict it. They upregulated E-flux transporter. I'll give you a big name. The abbreviation is ABCA1 transporter ATP binding cassette transporters. A1 is the one that evicts free cholesterol into certain protein molecules but there are other members of the ABC family which we don't have to really expand about now. So too much cholesterol gets evicted by an ABCA1 transporter and what is the protein that's accepting cholesterol from cells. These proteins that rapolipids are called apoprotines and once they accept lipids they're called apolipoprotines and they evolve into the full lipoprotein. So the apolipotine that accepts lipids from our peripheral cells is called apolprotein capital A dash 1 either arabak or rumen that Roman number 1. Apol1 is the structural protein of our high density lipoproteins are HDLs. So HDLs are the important lipoproteins that say okay Mr. Cell you got too much cholesterol I'll take it and I'll bring it somewhere else to spare you cholesterol toxicity. So the HDL when it accepts only free cholesterol but it was phospholipids that line the surface they carry two fatty acids don't they. So the HDL particle also carries an enzyme we'll call it L-cat because it's LCAT less than cholesterol acytransferase for the scientist listening to this podcast. So what that enzyme does is it takes one fatty acid off of the leg of a phospholipid and it attaches it to cholesterol for me cholesterol with a fatty acid cholesterol ester that's a incredibly hydrophobic water heating cholesterol molecule. So free cholesterol can actually sit on the surface of an HDL but if it gets a starfight it has to migrate to the core of the HDL. So that process keeps occurring and occurring and occurring as the HDApoA1 accepts more and more cholesterol and before you know it right before our eyes are HDL particle matures from a little flat bed truck to a discoid truck to a balloon and that is the mature fully cholesterol loaded HDL particle which can float around our plasma because APOA1 is soluble. Interesting the HDL's carry one two three four even five molecules of APOA1 and so say macro molecule as we're going to talk about the whole lipoprotein family it is by far the smallest compared to the other ones that are floating around and because it's small even though it's carrying a lot of molecules by the way most people are not taught this and it's one of these interesting fat toys if you ever do medical trivia. How many molecules of cholesterol are actually in each and every mature HDL particle? It's 45. You know it doesn't sound like a lot and that's why HDL's are so small. Yes they carry cholesterol but because there are quadrillions of HDL particles it doesn't matter that they're smaller like an army of ants that can carry a lot of stuff but their each one is tiny. When we first discovered lipoproteins in the 1940s the people who did that did it found separated them in a centrifuge. They took serum and they put it in the centrifuge and you know spun it around it was a big powerful ultra centrifuge. It's a centrifuge from over 24 hours and after that they saw there are distinct layers of lipoprotein particles so the first classification is they described them by their density. The ones that floated on top were called very low density lipoproteins. We know them today as VLDL's a little sunken to the tube was low density lipoproteins and on the bottom of the tube was the high density lipoproteins. Now what determines the buoyancy of these particles? It's like the same thing if you jump in a swimming pool fat people float more than skinny people who sent it at the bottom. So the HDL carries few lipids it's mostly proteins so it sinks it has a very high density and it's the name. The VLDL's are full of lipids they're big fat balloons so they float they don't sink very much at all and as they lose lipids they become smaller so their density gets a little lower because they're losing lipids and they become the low density lipoproteins. I did say hey lipids get into the intestine. The intestine does make its own lipoprotein which takes lipids into our plasma brings them to certain tissues or the liver. They're monstrous the biggest of our lipoproteins and they're called chylomycrons and they basically float in a centrifuge they're so fat so full of lipids. Yeah just float they don't sink at all. So we have chylomycrons very low density low density and high density. Trivia in between low density and very low density is a transient particle called intermediate density ideal. So I've just named all the lipoproteins to you. VLDL's chylos, ideals, LDL's and HDL's there are no others within each class each class is sort of a heterogeneous mixture of particles. Be turn them by their buoyancy. The big fat ones as they lose lipids become smaller smaller smaller so as a VLDL loses its lipids it gets to a point or you can't call it a VLDL anymore it becomes an ideal and the ideal rapidly loses some lipids and you can't call it an ideal anymore it becomes an LDL. That's our total family of lipoproteins. By the way we're going to talk a little bit about measuring lipid metrics in the laboratory. So one of the usually on the top of every lipid profile a person gets back is something called total cholesterol. Total cholesterol would be the laboratory has separated all of the lipoproteins and it assayed the cholesterol it's in each and every lipoprotein and added them together. Total cholesterol is basically VLDL cholesterol plus ideal cholesterol plus LDL cholesterol plus HDL cholesterol. So that's your total cholesterol metric. We don't get it in our laboratory reports but fancy labs could give you a VLDL cholesterol level by assaying the amount of cholesterol and VLDLs. A little while I'm going to tell you you're not going to get that reported to you but it's an easy calculation if you'd like to do it. Of course labs report LDL cholesterol to us. Most labs believe it or not they don't directly assay the cholesterol it's in your LDL particles. There's another mathematical formula that allows them to guess it. Hey a mathematical formulas are cheaper than buying reagents that can directly measure something. So that's called the calculated LDL cholesterol as opposed to a directly measured LDL cholesterol which does cost a little more money because the lab has the body's assays that just will give us that specific value. In general directly measured and calculated LDL cholesterol in physiologic circumstances have a high degree of accuracy. Concordance as it's called but unfortunately another topic we'll head into. Sometimes they are direct LDL cholesterol does not match the calculated that's called discordance and then you have to know do I believe the calculator do I breathe the direct more on that later and then of course the all labs directly measure the cholesterol that is in HDLs. So you have to directly measured HDL and total cholesterol VLDL cholesterol is a calculation but if you calculated VLDL cholesterol now if you took cholesterol total cholesterol and subtract it from it your VLDL cholesterol and your HDL cholesterol you would have your calculated LDL cholesterol level that's the formula that's that easy and I might as well get to it now because I want to jump back to the HDLs that have accepted cholesterol from yourself but the calculation for VLDL cholesterol was discovered in the mid 1970s by one of the gods of lipidology Dr. Frida Ward and he said listen VLDL's are mostly triglyceride carrying particles on average they carry five times more triglyceride than cholesterol almost all of the cholesterol that we measure in plasma is VLDL triglyceride. So if I take trig total triglyceride levels and the assumption that they're all in VLDL particles which is not exactly the truth. The third one we're talking in general terms here and divided it by five because there are five times more triglyceride and cholesterol I would calculate my VLDL cholesterol and then I have my equations subtracted calculated VLDL cholesterol the HDL cholesterol from total cholesterol what's left that's your LDL cholesterol you could see where that might go wrong is your triglyceride measurement too much or too little as the triglyceride levels go up up up that calculation becomes erroneous and therefore you're calculated it'll be all cholesterol becomes erroneous you know let's get away from clinical chemistry a bit unless you want me to lose it in any of the next I want to go back to the HDLs. If you're a woman in midlife or beyond you're probably noticed those changes in energy, strength and recovery just don't feel like they used to and what's frustrating is that for many women this happens even when you're eating well lifting weights prioritizing protein and doing all the right things you're not lazy you're not unmotivated and you're not doing anything wrong a big part of what's changing actually starts inside your cells as we age or mitochondria the energy producing structures inside our cells become less efficient and when mitochondrial function to clients it can show up as lower energy slower recovery reduce muscle strength and feeling less resilient overall this is a normal part of aging physiology and it's one of the reasons midlife can feel so different and that's why I've added might appear gummies from timeline nutrition into my daily routine might appears the only clinically proven form of uralithin A a compound shown in human clinical trials to support mitochondrial in simple terms it helps your cells do a better job of making energy and when your cells have more energy your body is able to support strength endurance and recovery as you age would I appreciate most that might appear is that it's foundational not flashy this isn't a stimulant or a quick fix it's a daily habit that supports how your body actually works at the cellular level and the gummies make it easy they're just two sugar free gummies per day they're vegan and cleanly formulated they're independently tested and certified for quality and if supporting your energy muscle health and overall resilience as you move through perimenopause and menopause is important to you might appear is worth considering you want to go to timelinenutrition.com slash Cynthia and use code Cynthia Thurlow for 20% off your order again that's timeline.com slash Cynthia and use code Cynthia Thurlow for 20% off your might appear gummies if you're in your 40s and 50s and feel like your body suddenly stop responding the way that it used to you're not imagining it bloating waking sleep disruptions food sensitivities and unpredictable energy are incredibly common in perimenopause and menopause but here's what most people aren't told your gut microbiome is changing right alongside your hormones and those changes can influence everything from how you store fat to how well you sleep to how your body processes estrogen that's exactly why I wrote my new book the menopause gut in this book I walk you through the science of how the microbiome metabolism immune system and hormones are all connected during midlife but most importantly I give you practical realistic strategies you can start using right away without extreme diets or complicated protocols you'll learn why the same diet that worked in your 30s may not work now how your gut influences hot flashes mood and weight the truth about fiber protein and blood sugar in midlife and the daily habits that help your body feel safe stable and resilient again if you're tired of blaming yourself for changes that are actually biological this book will help you understand what's really happening and what to do about it you can pre-order the menopause gut wherever books are sold and when you do be sure to check out the special pre-order bonuses I put together for you again you can go to www.synthethorlo.com you'll click on the banner it'll take you to multiple options for where you can order the menopause gut in presale yeah so out of curiosity you were indicating that as your triglycerides are going up it lessens the specificity of the calculated LDL where in literature the research or your clinical experience where is that number for triglycerides because I know when I was working in cardiology there were certain numbers and metrics we like to focus in on and triglycerides obviously were one of them but in your research and in your experience what is that number where you feel like it starts to lessen the power of that calculated LDL great question and listen when dr. Frito Wald event at the formula he warned there were shortcomings through it if you read the whole paper but you remember back in the 1970s and he's probably looking at 1960s blood from populations very different lipid concentrations in those people back then compared to us 50 60 70 years later for goodness eggs so and what happened is we developed insulin resistance in our population and one of the hallmark lipid abnormalities was raising triglycerides that's always a clue to a clinician that you're dealing with the insulin resistant prediabetic or diabetic the incidence of all of those are probably five times more than what they were in dr. Frito Wald's term it was diabetes was there but it was nowhere near the epidemic that it is now so do we answer your question so initially they said hey when the triglycerides hit 400 don't use that calculation and so you went to weren't that many who had triglycerides that were elevated back then but as guidelines involved in the first time they started giving us triglyceride numbers that had any accuracy we're in the late 90s around 2000 and they made the declaration that a triglyceride above 150 is high risk triglycerides that is certainly true but I would like your audience to know a trick of 150 is the 75th percent that means at a trigle 150 75 percent of the population has a triglyceride on their 150 and a lot of them are prediabetics and even early diabetic so obviously a trigle 150 is like burger or me vacuit the building as quickly as possible but I would like that burger long to go off when your trig is around 100 because that is where trig start getting into lipoproteins that they have no business being in and they distort whatever those lipoproteins are supposed to be doing and the particles they get into that they're not supposed to be in our LDLs and our HDLs and triglycerides starts invading an LDL or an HDL what gets knocked out cholesterol so as triglycerides goes up it's not uncommon to see LDL cholesterol going down but that's not a victory that's a nightmare and I'll explain while I keep saying I've got a lot of stuff to explain later but saying with the HDL an HDL students and carry no triglyceride molecules but if trig starts sneaking in and they do have a way of getting in the HDL garner more and more trig we don't measure HDL triglycerides but if we did we would see this but if trig is invading HDL what has to leave cholesterol I think everybody knows as trig goes up there's an inverse relationship with HDL cholesterol it goes down many people use the triglyceride HDL ratio and that ratio is basically trig's going up HDL cholesterol going down so the ratio goes up because HDLc is the denominator in that ratio. Dan Raider is the first to describe this and he used the term which I love as trig's invading HDL we should call them fat HDLs because it's like obese people they're you consider belly is carrying something it shouldn't well if trig's invading HDL they're getting fat and unfortunately they can't carry cholesterol which happens to be the major one of the big reasons HDL particles exist so using that I'm going to jump back I told you HDLs accept unwanted cholesterol from cells they have this enzyme LCAT that is sterifies it making the HDL a big balloon full of cholesterol ester almost no triglycerides in that molecule a couple but nothing of any concern now you have all these big gigantic HDLs floating around your plasma obviously you have to do something with that cholesterol they don't float forever and need actually one of the purposes of HDLs is to bring to cholesterol that was not wanted by cells and bring it to either an organ that can get rid of the excess cholesterol or bring it to some cells it might actually need some extra cholesterol so here are the avenues for mature HDL particles and by the way when they go to a cell that wants cholesterol they're going to be unloaded that's called delipidation when the cells pump cholesterol out and made the cholesterol's bigger the HDL's bigger bigger bigger that's called lipedation so a lipoprotein gaining lipids they lipidate they become bigger by the way what happens to their density when they become bigger density is lower they start floating a little higher and when they are delipidated they're not carrying lipids their density goes higher they sink in the centrifuge too i love applying physical chemistry to i hope it helps people understand some of these lipid mechanics and lipid processes that are occurring no and it's so interesting i think you know big pearl that you said is if 150 milligrams per desolate for triglyceride is considered to be you know high and helping people understand that that's you know 75th percentile we really need to be getting concern when we see the triglycerides creeping above 100 i usually say 75 but you know you are more more versed in the literature this is important for people to understand because just because you're lip you're total triglycerides or the triglycerides from your lipid panel are showing 140 and and you're probably being told that's okay what you're identifying is we need to get concerned when that triglyceride level is above 100 yes and you know i'm give you a pat on the back if i was going to be totally honest i said 100 because it's an i totally agree with you anything above 70 is not a physiologic triglyceride level a physiologic triglyceride is about 40 milligrams per desolate i going up to 70 is not going to hurt you too much but above that i'm going to tie this all together if you see a trig between 70 and 150 you at least ought to be thinking of am I dealing with early insulin resistance and or early ascvd risk and you are but i have to tell you why the triglycerides really cause atherosclerosis because atherosclerosis is accumulation of cholesterol in your artery wall it's not accumulation of triglycerides in your artery wall but as trig go up and we know insulin resistance people diabetic to your top of a acvd somehow the triglyceride must be modifying the particles that are carrying cholesterol that can crash your artery wall and that's going to be the final answer to this and that transformation starts to occur at very low triglyceride levels you know what's sad though Cynthia you would be told if your trig is one third or your normal that's not a sane statement to make but we actually have in certainly in your experience and in mind we've seen people who go in and have trig of 300 and are told don't worry about it oh my god hey look it's not all insulin resistance of course we can inherit genes that affect trigly but almost all of it in the real world is insulin resistance so but you can't ever dismiss a triglyceride level that is monstrous or even what you are being told because it's green on a lipid panel I wish they would get rid of these silly colors or adapt them to the modern it takes forever for that type of change to occur so but we're gonna tell you as part of our little lipid journey here why you should worry when you transfer about 75 it's interesting I was with a family member for Christmas and he was sharing his lipid results and he was getting ready to go on vacation and I said when you come back we need to sit down and talk because I think his triglycerides were 160 his LDL was fairly low you know his fasting glucose was in the high 90s and I just said you know we need to be doing more than what you're doing and so I think it's important for people to understand that there are definitely metrics we want to focus in on at an earlier stage unfortunately you know the research sometimes takes 10 15 20 years to sink into clinical practice and this is why this conversation is so important because we're dealing with a diabetes epidemic and there are far more people that are at risk that really have no idea yeah you did your brother in law favor they are by pointing that out to him and he should listen to this podcast won't get it up and then obviously come back and consult with you because that if we put him through an insulin clamp study or even a simpler glucose tolerance test demand has got serious dysmetabolic issues there if you think of the markers you even describe most people know what the metabolic syndrome is he doesn't quite meet the criteria there but you could see he's on his way to reaching full-blown metabolic syndrome and no doubt that has been sneaking up on him for a decade or two it's not like it occurred last week and for a decade or two his arteries have been subject to some bad stuff takes a long time for at thrice grotesces to put us in a graveyard but if we knew this stuff was happened at an early age we might ultimately live longer live healthier ultimately die of something else there's no need to die of a scb-d or dysmetabolic diseases so yeah so we you have to learn some of the new numbers there if you love this podcast episode please leave a rating and review subscribe and tell a friend